Mink S, Haenig B, Klempnauer K H
Hans Spemann Laboratory, Max Planck Institute for Immunobiology, Freiburg, Germany.
Mol Cell Biol. 1997 Nov;17(11):6609-17. doi: 10.1128/MCB.17.11.6609.
Transcriptional coactivators such as p300 and CREB-binding protein (CBP) function as important elements in the transcription factor network, linking individual transactivators via protein-protein interactions to the basal transcriptional machinery. We have investigated whether p300 plays a role in transactivation mediated by C/EBPbeta, a conserved member of the C/EBP family. We show that C/EBPbeta-dependent transactivation is strongly inhibited by adenovirus E1A but not by E1A mutants defective in p300 binding. Ectopic expression of p300 reverses the E1A-dependent inhibition and increases the transactivation potential of C/EBPbeta. Furthermore, we show that C/EBPbeta and p300 interact with each other and demonstrate that the sequences responsible for interaction map to the E1A binding region of p300 and the amino terminus of C/EBPbeta. Finally, we show that the minimal C/EBPbeta binding site of p300 acts as a dominant-negative inhibitor of C/EBPbeta. These observations identify p300 as a bona fide coactivator for C/EBPbeta. C/EBPbeta is highly expressed in the myelomonocytic lineage of the hematopoietic system and cooperates with Myb to activate mim-1, a gene specifically expressed during myelomonocytic differentiation. Recent evidence has shown that Myb recruits CBP (and presumably p300) as a coactivator and, in contrast to C/EBPbeta, interacts with the CREB binding site of p300-CBP. We show that p300 not only stimulates the activity of Myb and C/EBPbeta individually but also increases the synergy between them. Thus, our results reveal a novel function of p300: in addition to linking specific transcription factors to the basal transcriptional machinery, p300 also mediates the cooperation between transactivators interacting with different domains of p300.
转录共激活因子如p300和CREB结合蛋白(CBP)在转录因子网络中发挥重要作用,通过蛋白质-蛋白质相互作用将单个转录激活因子与基础转录机制联系起来。我们研究了p300是否在由C/EBPβ介导的反式激活中发挥作用,C/EBPβ是C/EBP家族的一个保守成员。我们发现,腺病毒E1A强烈抑制C/EBPβ依赖性反式激活,但与p300结合缺陷的E1A突变体无关。p300的异位表达可逆转E1A依赖性抑制并增加C/EBPβ的反式激活潜能。此外,我们表明C/EBPβ和p300相互作用,并证明负责相互作用的序列定位于p300的E1A结合区域和C/EBPβ的氨基末端。最后,我们表明p300的最小C/EBPβ结合位点作为C/EBPβ的显性负抑制剂发挥作用。这些观察结果确定p300是C/EBPβ的真正共激活因子。C/EBPβ在造血系统的髓单核细胞谱系中高度表达,并与Myb协同激活mim-1,mim-1是在髓单核细胞分化过程中特异性表达的基因。最近的证据表明,Myb招募CBP(可能还有p300)作为共激活因子,并且与C/EBPβ不同,Myb与p300-CBP的CREB结合位点相互作用。我们表明,p300不仅单独刺激Myb和C/EBPβ的活性,还增加它们之间的协同作用。因此,我们的结果揭示了p300的一种新功能:除了将特定转录因子与基础转录机制联系起来外,p300还介导与p300不同结构域相互作用的转录激活因子之间的合作。